Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms
Aims To evaluate whether the potent hypophagic and weight‐suppressive effects of growth differentiation factor‐15 (GDF15) and semaglutide combined would be a more efficacious antiobesity treatment than either treatment alone by examining whether the neural and behavioural mechanisms contributing to...
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| Veröffentlicht in: | Diabetes, obesity & metabolism obesity & metabolism, 2022-06, Vol.24 (6), p.1010-1020 |
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| creator | Ghidewon, M. Wald, H.S. McKnight, A. D. De Jonghe, B. C. Breen, D. M. Alhadeff, A. L. Borner, T. Grill, H. J. |
| description | Aims
To evaluate whether the potent hypophagic and weight‐suppressive effects of growth differentiation factor‐15 (GDF15) and semaglutide combined would be a more efficacious antiobesity treatment than either treatment alone by examining whether the neural and behavioural mechanisms contributing to their anorectic effects were common or disparate.
Materials/Methods
Three mechanisms were investigated to determine how GDF15 and semaglutide induce anorexia: the potentiation of the intake suppression by gastrointestinal satiation signals; the reduction in motivation to feed; and the induction of visceral malaise. We then compared the effects of short‐term, combined GDF15 and semaglutide treatment on weight loss to the individual treatments. Rat pharmaco‐behavioural experiments assessed whether GDF15 or semaglutide added to the satiating effects of orally gavaged food and exogenous cholecystokinin (CCK). A progressive ratio operant paradigm was used to examine whether GDF15 or semaglutide reduced feeding motivation. Pica behaviour (ie, kaolin intake) and conditioned affective food aversion testing were used to evaluate visceral malaise. Additionally, fibre photometry studies were conducted in agouti‐related protein (AgRP)‐Cre mice to examine whether GDF15 or semaglutide, alone or in combination with CCK, modulate calcium signalling in hypothalamic AgRP neurons.
Results
Semaglutide reduced food intake by amplifying the feeding‐inhibitory effect of CCK or ingested food, inhibited the activity of AgRP neurons when combined with CCK, reduced feeding motivation and induced malaise. GDF15 induced visceral malaise but, strikingly, did not affect feeding motivation, the satiating effect of ingested food or CCK signal processing. Combined GDF15 and semaglutide treatment produced greater food intake and body weight suppression than did either treatment alone, without enhancing malaise.
Conclusions
GDF15 and semaglutide reduce food intake and body weight through largely distinct processes that produce greater weight loss and feeding suppression when combined. |
| doi_str_mv | 10.1111/dom.14663 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9796095</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2626230371</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4433-8f39f02b6626f56ced562af35ee8b8f17530d9b8ce4b5e082fc3760bcbb98aa53</originalsourceid><addsrcrecordid>eNp1kctu1DAUhiMEoqWw4AWQJTatRFpfEifZIKFeBqSibmBt-XKcuCRxsZ2O5hV46npmSgVIeHNs-dN3ztFfFG8JPiX5nBk_nZKKc_asOMyVlYRR_nx3p2XbYXpQvIrxFmNcsbZ5WRywmtCO8uqw-LUKfp0GZJy1EGBOTibnZ2SlTj4gUqPj1cUVqU-QnA2KMMl-XJIzgNw8OOUSst6b_EjyB-wY5c0GrcH1Q0JpCH7pBzTK0MO4yV1icrNOH5A0xiV3D2gCPcjZxSm-Ll5YOUZ481iPiu9Xl9_OP5fXN6sv55-uS11VjJWtZZ3FVHFOua25BlNzKi2rAVrVWtLUDJtOtRoqVQNuqdWs4VhppbpWypodFR_33rtFTWB0XjrIUdwFN8mwEV468ffP7AbR-3vRNR3H3VZw_CgI_ucCMYnJRQ3jKGfwSxQ0T0YZZg3J6Pt_0Fu_hDmvl6maVrjieCs82VM6-BgD2KdhCBbbhEVOWOwSzuy7P6d_In9HmoGzPbB2I2z-bxIXN1_3ygcCg7Ir</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2652404605</pqid></control><display><type>article</type><title>Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Ghidewon, M. ; Wald, H.S. ; McKnight, A. D. ; De Jonghe, B. C. ; Breen, D. M. ; Alhadeff, A. L. ; Borner, T. ; Grill, H. J.</creator><creatorcontrib>Ghidewon, M. ; Wald, H.S. ; McKnight, A. D. ; De Jonghe, B. C. ; Breen, D. M. ; Alhadeff, A. L. ; Borner, T. ; Grill, H. J.</creatorcontrib><description>Aims
To evaluate whether the potent hypophagic and weight‐suppressive effects of growth differentiation factor‐15 (GDF15) and semaglutide combined would be a more efficacious antiobesity treatment than either treatment alone by examining whether the neural and behavioural mechanisms contributing to their anorectic effects were common or disparate.
Materials/Methods
Three mechanisms were investigated to determine how GDF15 and semaglutide induce anorexia: the potentiation of the intake suppression by gastrointestinal satiation signals; the reduction in motivation to feed; and the induction of visceral malaise. We then compared the effects of short‐term, combined GDF15 and semaglutide treatment on weight loss to the individual treatments. Rat pharmaco‐behavioural experiments assessed whether GDF15 or semaglutide added to the satiating effects of orally gavaged food and exogenous cholecystokinin (CCK). A progressive ratio operant paradigm was used to examine whether GDF15 or semaglutide reduced feeding motivation. Pica behaviour (ie, kaolin intake) and conditioned affective food aversion testing were used to evaluate visceral malaise. Additionally, fibre photometry studies were conducted in agouti‐related protein (AgRP)‐Cre mice to examine whether GDF15 or semaglutide, alone or in combination with CCK, modulate calcium signalling in hypothalamic AgRP neurons.
Results
Semaglutide reduced food intake by amplifying the feeding‐inhibitory effect of CCK or ingested food, inhibited the activity of AgRP neurons when combined with CCK, reduced feeding motivation and induced malaise. GDF15 induced visceral malaise but, strikingly, did not affect feeding motivation, the satiating effect of ingested food or CCK signal processing. Combined GDF15 and semaglutide treatment produced greater food intake and body weight suppression than did either treatment alone, without enhancing malaise.
Conclusions
GDF15 and semaglutide reduce food intake and body weight through largely distinct processes that produce greater weight loss and feeding suppression when combined.</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.14663</identifier><identifier>PMID: 35129264</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Agouti-Related Protein - metabolism ; animal pharmacology ; Animals ; Anorexia ; Anorexia - drug therapy ; Anorexia - metabolism ; Antidiabetics ; antiobesity drug ; appetite control ; Body weight ; Body Weight - drug effects ; Body weight loss ; Calcium signalling ; Cholecystokinin ; Cholecystokinin - metabolism ; Drug therapy ; Eating - drug effects ; Feeding behavior ; Food ; Food aversion ; Food intake ; Food processing ; GLP‐1 analogue ; Glucagon-Like Peptides - pharmacology ; Growth Differentiation Factor 15 - pharmacology ; Hypothalamus ; Kaolin ; Mice ; Motivation ; neuropharmacology ; Obesity ; Operant conditioning ; Photometry ; Potentiation ; Rats ; Satiety ; Signal processing ; Weight ; Weight control ; Weight Loss - drug effects</subject><ispartof>Diabetes, obesity & metabolism, 2022-06, Vol.24 (6), p.1010-1020</ispartof><rights>2022 John Wiley & Sons Ltd.</rights><rights>2022 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4433-8f39f02b6626f56ced562af35ee8b8f17530d9b8ce4b5e082fc3760bcbb98aa53</citedby><cites>FETCH-LOGICAL-c4433-8f39f02b6626f56ced562af35ee8b8f17530d9b8ce4b5e082fc3760bcbb98aa53</cites><orcidid>0000-0002-6980-5355 ; 0000-0001-9438-695X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdom.14663$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdom.14663$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35129264$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ghidewon, M.</creatorcontrib><creatorcontrib>Wald, H.S.</creatorcontrib><creatorcontrib>McKnight, A. D.</creatorcontrib><creatorcontrib>De Jonghe, B. C.</creatorcontrib><creatorcontrib>Breen, D. M.</creatorcontrib><creatorcontrib>Alhadeff, A. L.</creatorcontrib><creatorcontrib>Borner, T.</creatorcontrib><creatorcontrib>Grill, H. J.</creatorcontrib><title>Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>Aims
To evaluate whether the potent hypophagic and weight‐suppressive effects of growth differentiation factor‐15 (GDF15) and semaglutide combined would be a more efficacious antiobesity treatment than either treatment alone by examining whether the neural and behavioural mechanisms contributing to their anorectic effects were common or disparate.
Materials/Methods
Three mechanisms were investigated to determine how GDF15 and semaglutide induce anorexia: the potentiation of the intake suppression by gastrointestinal satiation signals; the reduction in motivation to feed; and the induction of visceral malaise. We then compared the effects of short‐term, combined GDF15 and semaglutide treatment on weight loss to the individual treatments. Rat pharmaco‐behavioural experiments assessed whether GDF15 or semaglutide added to the satiating effects of orally gavaged food and exogenous cholecystokinin (CCK). A progressive ratio operant paradigm was used to examine whether GDF15 or semaglutide reduced feeding motivation. Pica behaviour (ie, kaolin intake) and conditioned affective food aversion testing were used to evaluate visceral malaise. Additionally, fibre photometry studies were conducted in agouti‐related protein (AgRP)‐Cre mice to examine whether GDF15 or semaglutide, alone or in combination with CCK, modulate calcium signalling in hypothalamic AgRP neurons.
Results
Semaglutide reduced food intake by amplifying the feeding‐inhibitory effect of CCK or ingested food, inhibited the activity of AgRP neurons when combined with CCK, reduced feeding motivation and induced malaise. GDF15 induced visceral malaise but, strikingly, did not affect feeding motivation, the satiating effect of ingested food or CCK signal processing. Combined GDF15 and semaglutide treatment produced greater food intake and body weight suppression than did either treatment alone, without enhancing malaise.
Conclusions
GDF15 and semaglutide reduce food intake and body weight through largely distinct processes that produce greater weight loss and feeding suppression when combined.</description><subject>Agouti-Related Protein - metabolism</subject><subject>animal pharmacology</subject><subject>Animals</subject><subject>Anorexia</subject><subject>Anorexia - drug therapy</subject><subject>Anorexia - metabolism</subject><subject>Antidiabetics</subject><subject>antiobesity drug</subject><subject>appetite control</subject><subject>Body weight</subject><subject>Body Weight - drug effects</subject><subject>Body weight loss</subject><subject>Calcium signalling</subject><subject>Cholecystokinin</subject><subject>Cholecystokinin - metabolism</subject><subject>Drug therapy</subject><subject>Eating - drug effects</subject><subject>Feeding behavior</subject><subject>Food</subject><subject>Food aversion</subject><subject>Food intake</subject><subject>Food processing</subject><subject>GLP‐1 analogue</subject><subject>Glucagon-Like Peptides - pharmacology</subject><subject>Growth Differentiation Factor 15 - pharmacology</subject><subject>Hypothalamus</subject><subject>Kaolin</subject><subject>Mice</subject><subject>Motivation</subject><subject>neuropharmacology</subject><subject>Obesity</subject><subject>Operant conditioning</subject><subject>Photometry</subject><subject>Potentiation</subject><subject>Rats</subject><subject>Satiety</subject><subject>Signal processing</subject><subject>Weight</subject><subject>Weight control</subject><subject>Weight Loss - drug effects</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctu1DAUhiMEoqWw4AWQJTatRFpfEifZIKFeBqSibmBt-XKcuCRxsZ2O5hV46npmSgVIeHNs-dN3ztFfFG8JPiX5nBk_nZKKc_asOMyVlYRR_nx3p2XbYXpQvIrxFmNcsbZ5WRywmtCO8uqw-LUKfp0GZJy1EGBOTibnZ2SlTj4gUqPj1cUVqU-QnA2KMMl-XJIzgNw8OOUSst6b_EjyB-wY5c0GrcH1Q0JpCH7pBzTK0MO4yV1icrNOH5A0xiV3D2gCPcjZxSm-Ll5YOUZ481iPiu9Xl9_OP5fXN6sv55-uS11VjJWtZZ3FVHFOua25BlNzKi2rAVrVWtLUDJtOtRoqVQNuqdWs4VhppbpWypodFR_33rtFTWB0XjrIUdwFN8mwEV468ffP7AbR-3vRNR3H3VZw_CgI_ucCMYnJRQ3jKGfwSxQ0T0YZZg3J6Pt_0Fu_hDmvl6maVrjieCs82VM6-BgD2KdhCBbbhEVOWOwSzuy7P6d_In9HmoGzPbB2I2z-bxIXN1_3ygcCg7Ir</recordid><startdate>202206</startdate><enddate>202206</enddate><creator>Ghidewon, M.</creator><creator>Wald, H.S.</creator><creator>McKnight, A. D.</creator><creator>De Jonghe, B. C.</creator><creator>Breen, D. M.</creator><creator>Alhadeff, A. L.</creator><creator>Borner, T.</creator><creator>Grill, H. J.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6980-5355</orcidid><orcidid>https://orcid.org/0000-0001-9438-695X</orcidid></search><sort><creationdate>202206</creationdate><title>Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms</title><author>Ghidewon, M. ; Wald, H.S. ; McKnight, A. D. ; De Jonghe, B. C. ; Breen, D. M. ; Alhadeff, A. L. ; Borner, T. ; Grill, H. J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4433-8f39f02b6626f56ced562af35ee8b8f17530d9b8ce4b5e082fc3760bcbb98aa53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Agouti-Related Protein - metabolism</topic><topic>animal pharmacology</topic><topic>Animals</topic><topic>Anorexia</topic><topic>Anorexia - drug therapy</topic><topic>Anorexia - metabolism</topic><topic>Antidiabetics</topic><topic>antiobesity drug</topic><topic>appetite control</topic><topic>Body weight</topic><topic>Body Weight - drug effects</topic><topic>Body weight loss</topic><topic>Calcium signalling</topic><topic>Cholecystokinin</topic><topic>Cholecystokinin - metabolism</topic><topic>Drug therapy</topic><topic>Eating - drug effects</topic><topic>Feeding behavior</topic><topic>Food</topic><topic>Food aversion</topic><topic>Food intake</topic><topic>Food processing</topic><topic>GLP‐1 analogue</topic><topic>Glucagon-Like Peptides - pharmacology</topic><topic>Growth Differentiation Factor 15 - pharmacology</topic><topic>Hypothalamus</topic><topic>Kaolin</topic><topic>Mice</topic><topic>Motivation</topic><topic>neuropharmacology</topic><topic>Obesity</topic><topic>Operant conditioning</topic><topic>Photometry</topic><topic>Potentiation</topic><topic>Rats</topic><topic>Satiety</topic><topic>Signal processing</topic><topic>Weight</topic><topic>Weight control</topic><topic>Weight Loss - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ghidewon, M.</creatorcontrib><creatorcontrib>Wald, H.S.</creatorcontrib><creatorcontrib>McKnight, A. D.</creatorcontrib><creatorcontrib>De Jonghe, B. C.</creatorcontrib><creatorcontrib>Breen, D. M.</creatorcontrib><creatorcontrib>Alhadeff, A. L.</creatorcontrib><creatorcontrib>Borner, T.</creatorcontrib><creatorcontrib>Grill, H. J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ghidewon, M.</au><au>Wald, H.S.</au><au>McKnight, A. D.</au><au>De Jonghe, B. C.</au><au>Breen, D. M.</au><au>Alhadeff, A. L.</au><au>Borner, T.</au><au>Grill, H. J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2022-06</date><risdate>2022</risdate><volume>24</volume><issue>6</issue><spage>1010</spage><epage>1020</epage><pages>1010-1020</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><abstract>Aims
To evaluate whether the potent hypophagic and weight‐suppressive effects of growth differentiation factor‐15 (GDF15) and semaglutide combined would be a more efficacious antiobesity treatment than either treatment alone by examining whether the neural and behavioural mechanisms contributing to their anorectic effects were common or disparate.
Materials/Methods
Three mechanisms were investigated to determine how GDF15 and semaglutide induce anorexia: the potentiation of the intake suppression by gastrointestinal satiation signals; the reduction in motivation to feed; and the induction of visceral malaise. We then compared the effects of short‐term, combined GDF15 and semaglutide treatment on weight loss to the individual treatments. Rat pharmaco‐behavioural experiments assessed whether GDF15 or semaglutide added to the satiating effects of orally gavaged food and exogenous cholecystokinin (CCK). A progressive ratio operant paradigm was used to examine whether GDF15 or semaglutide reduced feeding motivation. Pica behaviour (ie, kaolin intake) and conditioned affective food aversion testing were used to evaluate visceral malaise. Additionally, fibre photometry studies were conducted in agouti‐related protein (AgRP)‐Cre mice to examine whether GDF15 or semaglutide, alone or in combination with CCK, modulate calcium signalling in hypothalamic AgRP neurons.
Results
Semaglutide reduced food intake by amplifying the feeding‐inhibitory effect of CCK or ingested food, inhibited the activity of AgRP neurons when combined with CCK, reduced feeding motivation and induced malaise. GDF15 induced visceral malaise but, strikingly, did not affect feeding motivation, the satiating effect of ingested food or CCK signal processing. Combined GDF15 and semaglutide treatment produced greater food intake and body weight suppression than did either treatment alone, without enhancing malaise.
Conclusions
GDF15 and semaglutide reduce food intake and body weight through largely distinct processes that produce greater weight loss and feeding suppression when combined.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>35129264</pmid><doi>10.1111/dom.14663</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-6980-5355</orcidid><orcidid>https://orcid.org/0000-0001-9438-695X</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1462-8902 |
| ispartof | Diabetes, obesity & metabolism, 2022-06, Vol.24 (6), p.1010-1020 |
| issn | 1462-8902 1463-1326 |
| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Agouti-Related Protein - metabolism animal pharmacology Animals Anorexia Anorexia - drug therapy Anorexia - metabolism Antidiabetics antiobesity drug appetite control Body weight Body Weight - drug effects Body weight loss Calcium signalling Cholecystokinin Cholecystokinin - metabolism Drug therapy Eating - drug effects Feeding behavior Food Food aversion Food intake Food processing GLP‐1 analogue Glucagon-Like Peptides - pharmacology Growth Differentiation Factor 15 - pharmacology Hypothalamus Kaolin Mice Motivation neuropharmacology Obesity Operant conditioning Photometry Potentiation Rats Satiety Signal processing Weight Weight control Weight Loss - drug effects |
| title | Growth differentiation factor 15 (GDF15) and semaglutide inhibit food intake and body weight through largely distinct, additive mechanisms |
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